L773:0960 314X OR L773:1473 561X
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| Fältnamn | Indikatorer | Metadata |
|---|---|---|
| 000 | 03097naa a2200337 4500 | |
| 001 | oai:DiVA.org:uu-54712 | |
| 003 | SwePub | |
| 008 | 080118s2000 | |||||||||||000 ||eng| | |
| 024 | 7 | a https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-547122 URI |
| 040 | a (SwePub)uu | |
| 041 | a engb eng | |
| 042 | 9 SwePub | |
| 072 | 7 | a ref2 swepub-contenttype |
| 072 | 7 | a art2 swepub-publicationtype |
| 100 | 1 | a Wadelius, Miau Uppsala universitet,Klinisk farmakogenomik och osteoporos4 aut0 (Swepub:uu)miawadel |
| 245 | 1 0 | a Polymorphisms of NAT2 in relation to sulphasalazine-induced agranulocytosis |
| 264 | 1 | c 2000 |
| 338 | a print2 rdacarrier | |
| 520 | a Agranulocytosis is a rare, but serious adverse reaction to sulphasalazine. The polymorphic enzyme N-acetyltransferase 2 (NAT2) plays an important role in the metabolism of sulphasalazine. This study was conducted to analyse whether the risk of sulphasalazine-induced agranulocytosis is increased in slow acetylators. Patients were treated for inflammatory disease, mostly joint disease, with a mean dose of 2 g sulphasalazine daily. Thirty-nine patients reacted with agranulocytosis, while 75 patients had been treated for a minimum of 3 months without haematological side-effects. A population-based control panel of 448 individuals was used for comparison. All subjects were genotyped for NAT2 by polymerase chain reaction followed by restriction enzyme digestion. The six most common allelic variants were analysed: NAT2*4, NAT2*5A, NAT2*5B, NAT2*5C, NAT2*6 and NAT2*7. The proportion of slow acetylators was significantly higher in patients with sulphasalazine-induced agranulocytosis (69%) and population-based controls (64%) compared to patients who tolerated sulphasalazine (45%); odds ratio 2.71 [95% confidence interval (CI) 1.20; 6.15], P = 0.015, and odds ratio 2.17 (95% CI 1.32; 3.56), P = 0.002, respectively. Patients who developed agranulocytosis did not differ from population-based control subjects in the frequency of slow acetylators; odds ratio 1.25 (95% CI 0.62; 2.53), P = 0.535. The risk of agranulocytosis did not appear to be increased in slow acetylators, provided that the difference compared with sulphasalazine-treated control subjects was not due to a predominance of fast acetylators among patients with inflammatory joint disease. Instead, selection bias was suspected since more slow acetylators may have discontinued sulphasalazine therapy because of drug-intolerance. | |
| 653 | a sulfasalazine | |
| 653 | a agranulocytosis | |
| 653 | a NAT2 | |
| 653 | a pharmacogenetics | |
| 653 | a MEDICINE | |
| 653 | a MEDICIN | |
| 700 | 1 | a Stjernberg, Elisabethu Uppsala universitet,Klinisk farmakologi4 aut |
| 700 | 1 | a Wiholm, Bengt-Erik4 aut |
| 700 | 1 | a Rane, Andersu Uppsala universitet,Institutionen för medicinska vetenskaper,Klinisk farmakologi, A Rane4 aut |
| 710 | 2 | a Uppsala universitetb Klinisk farmakogenomik och osteoporos4 org |
| 773 | 0 | t Pharmacogeneticsg 10:1, s. 35-41q 10:1<35-41x 0960-314Xx 1473-561X |
| 856 | 4 8 | u https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-54712 |
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